Polioencephalomalacia
Polioencephalomalacia is a thiamine-responsive disease
of ruminants. It was first described as thiaminedeficiency,
however, more recent evidence indicates that the disease
actually results from a disturbance in thiamine metabolism.
Proposed mechanisms include increased numbers of thiaminase
producing bacteria in the rumen, production or ingestion
of thiamine analogs, ingestion of thiaminases (as in bracken
fem), impaired thiamine absorption, and increased excretion
of thiamine. Animals on high-concentrate diets are at greater
risk of developing the disease, presumably because the low
rumen pH decreases the numbers of thiamine-producing bacteria
and increases the numbers of thiaminase producing bacteria.
High sulfur diets, amprolium, thiobendazole and levamisolehydrochloride
use have also been associated with this disorder. Clinical
signs of polioencephalo-malacia range from dullness, head
pressing and blindness to opisthotonus, muscle tremors,
twitching, hypersalivation, coma and death. Antemortem
confirmation of a diagnosis of Polioencephalomalacia is
difficult. The best indicator may be measurement of the
thiamine-dependent enzyme, erythrocytetransketolase. Levels
of this enzyme are a relatively sensitive and specific indicator
of active thiamine levels. The test compares the levels
of the active enzyme to its inactive form. In animals with
Polioencephalomalacia, the levels of the inactive enzyme
are increased. Rumen content analysis that shows a decrease
in gram-positive cocci and coccobacilli and an increase
in gram-positive bacilli is also indicative of deranged
thiamine metabolism. Looking for decreased thiamine pyro-phospate
levels in erythrocytes or rumen fluid may be useful. However,
decreases are not always seen in polioencephalomalaciaand
therefore, these tests are unreliable. Thiaminase may be
measured in the rumen and feces of affected animals,
Gross lesions of polioencephalomalacia include swelling
of the cerebrum, evidenced by flattened gyri and shallow
sulci. The cerebral cortex may be thinned. The distribution
is symmetrical. On cut section, a pale layer may be visible
near the junction of the gray and white matter. The affected
areas of cortex will fluoresce under UV light.
Histological lesions include laminar necrosis of cerebral
neuronal cell bodies. The deeper layers are more severely
affected. The neurons appear shrunken and eosinophilic,
and are surrounded by a clear space. Spongiosis is evident
in the cortex and the white matter immediately adjacent
to the cortex. Vessels in the meninges are often congested
with small to moderate accumulations of leukocytes. If the
animal survives over a week, liquefactive necrosis is evident
in the affected areas. The necrotic tissue is eventually
removed by phagocytes.
Differential diagnoses that should be considered for the
clinical signs of polio- encephalomalacia include rabies,
lead or other heavy metal poisoning, vitamin A deficiency,
ethyleneglycol intoxication, EBR encephalitis (in young
calves), and salt poisoning. If a presumptive diagnosis
of polioencephalomalacia can be made based on history, treatment
should be initiated to prevent further cerebral necrosis.
If diagnosed and treated early in the course of the disease,
affected animals may recover completely with treatment.
Thiamine (10-20 mg/kg) is administered intramuscularly or
subcutaneously three times a day. If it is necessary
to administer the initial treatment intravenously, it must
be diluted in an isotonic fluid and administered slowly.
Some animals may require concurrent therapy for convulsions.
Improvement is usually evident within 24 hours of treatment,
however, severely affected animals may require up to
one week to recover. Blindness may be permanent in these
animals.
Polioencephalomalacia may be prevented by supplementing
thiamine in the ration. Ruminants should be adapted slowly
to new diets. Cobalt supplementation may be necessary in
deficient areas. Calcium sulfate supplement, high-sulfur
sources of water, such as well-water, should be avoided
in the diet.
- byDianeFeutz Norton, Class of 1998
- edited by Lydia
Andrews-Jones, DVM
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